ArticleCell cycle (Georgetown, Tex.)2012
The specific role of pRb in p16 (INK4A) -mediated arrest of normal and malignant human breast cells.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Senescent endothelial cells: key commanders of the cellular communication network within atherosclerotic plaques.Frontiers in immunology · 2026Review
- Atrial myocyte senescence as a driver of atrial fibrillation: mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- P16 Expression in Human Breast Carcinoma and its Relationship to Clinicopathological Parameters.Advanced biomedical research · 2023Article
- Aberrant activation of p53/p66Shc-mInsc axis increases asymmetric divisions and attenuates proliferation of aged mammary stem cells.Cell death and differentiation · 2022Article
- p16 controls epithelial cell growth and suppresses carcinogenesis through mechanisms that do not require RB1 function.Oncogenesis · 2017Article
- The Potential Role of Senescence As a Modulator of Platelets and Tumorigenesis.Frontiers in oncology · 2017Article
- Palbociclib - from Bench to Bedside and Beyond.Breast care (Basel, Switzerland) · 2016Review
- Both Complexity and Location of DNA Damage Contribute to Cellular Senescence Induced by Ionizing Radiation.PloS one · 2016Article
- A TORC2-Akt Feed-Forward Topology Underlies HER3 Resiliency in HER2-Amplified Cancers.Molecular cancer therapeutics · 2015Article
- Therapeutic targeting of replicative immortality.Seminars in cancer biology · 2015Review
- Expression of p16 and pRB in invasive breast cancer.International journal of clinical and experimental pathology · 2015Article
- Relationships among folate, alcohol consumption, gene variants in one-carbon metabolism and p16INK4a methylation and expression in healthy breast tissues.Carcinogenesis · 2015Article
- Deregulation of the EGFR/PI3K/PTEN/Akt/mTORC1 pathway in breast cancer: possibilities for therapeutic intervention.Oncotarget · 2014Review
- Breast cancer risk after radiotherapy for heritable and non-heritable retinoblastoma: a US-UK study.British journal of cancer · 2014Article
- Inhibition of GSK-3β activity can result in drug and hormonal resistance and alter sensitivity to targeted therapy in MCF-7 breast cancer cells.Cell cycle (Georgetown, Tex.) · 2014Article
- Reinforcing targeted therapeutics with phenotypic stability factors.Cell cycle (Georgetown, Tex.) · 2014Article
- CDK4/6-inhibiting drug substitutes for p21 and p16 in senescence: duration of cell cycle arrest and MTOR activity determine geroconversion.Cell cycle (Georgetown, Tex.) · 2013Article
- Ras-induced ROS upregulation affecting cell proliferation is connected with cell type-specific alterations of HSF1/SESN3/p21Cip1/WAF1 pathways.Cell cycle (Georgetown, Tex.) · 2013Article
- Pluripotent stem cells escape from senescence-associated DNA methylation changes.Genome research · 2013Article
- pRb or its cousins: who controls the family business?Cell cycle (Georgetown, Tex.) · 2012Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
RB family proteins pRb, p107 and p130 have similar structures and overlapping functions, enabling cell cycle arrest and cellular senescence. pRb, but not p107 or p130, is frequently mutated in human malignancies. In human fibroblasts acutely exposed to oncogenic ras, pRb has a specific role in suppressing DNA replication, and p107 or p130 cannot compensate for the loss of this function; however, a second p53/p21-dependent checkpoint prevents escape from growth arrest. This model of oncogene-induced senescence requires the additional loss of p53/p21 to explain selection for preferential loss of pRb function in human malignancies. We asked whether similar rules apply to the role of pRb in growth arrest of human epithelial cells, the source of most cancers. In two malignant human breast cancer cell lines, we found that individual RB family proteins were sufficient for the establishment of p16-initiated senescence, and that growth arrest in G 1 was not dependent on the presence of functional pRb or p53. However, senescence induction by endogenous p16 was delayed in primary normal human mammary epithelial cells with reduced pRb but not with reduced p107 or p130. Thus, under these circumstances, despite the presence of functional p53, p107 and p130 were unable to completely compensate for pRb in mediating senescence induction. We propose that early inactivation of pRb in pre-malignant breast cells can, by itself, extend proliferative lifespan, allowing acquisition of additional changes necessary for malignant transformation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.